No evidence of non-homologous insertions in mouse model of MDD created by replacement of homologous mouse DNA sequence with pathogenic 6-base human CREB1 promoter sequence.
No evidence of non-homologous insertions in mouse model of MDD created by replacement of homologous mouse DNA sequence with pathogenic 6-base human CREB1 promoter sequence.
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没有证据表明 MDD 小鼠模型中存在非同源插入，该模型是通过用致病性 6 碱基人 CREB1 启动子序列替换同源小鼠 DNA 序列而创建的。
DOI：
10.1002/ajmg.b.32006
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发表时间：
2012
期刊：
影响因子：
--
通讯作者：
Hughes3rd,HughB
中科院分区：
文献类型：
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作者：
Zubenko,GeorgeS;Hughes3rd,HughB
我们最近报道了第一个基于病因学的重性抑郁症（MDD）重组小鼠模型的建立和初步表征。这是通过将相应的小鼠DNA序列替换为来自人类CREB 1启动子的6个碱基的DNA序列来实现的，该启动子与复发性早发性MDD先证者鉴定的家族中MDD的发生相关。本研究探讨了导致小鼠模型创建的mouseCreb1基因处的期望同源重组事件是否也伴随着靶向载体在小鼠基因组中非预期非同源位置的插入。在除mouseCreb1基因以外的区域未观察到靶向载体序列插入的证据。© 2011 Wiley Periodicals，Inc.
We have recently reported the creation and initial characterization of the first etiology‐based recombinant mouse model of major depressive disorder (MDD). This was achieved by replacing the corresponding mouse DNA sequence with a 6‐base DNA sequence from the humanCREB1promoter that is associated with the development of MDD in families identified by probands with recurrent, early‐onset MDD. The current study explored whether the desired homologous recombination event at the mouseCreb1gene that resulted in the creation of the mouse model was also accompanied by insertions of the targeting vector at unintended non‐homologous locations in the mouse genome. No evidence of insertions of targeting vector sequence was observed at regions other than the mouseCreb1gene. © 2011 Wiley Periodicals, Inc.